In our previous study, using a mouse model of ascending urinary tract infection, we have demonstrated the comparable pro-inflammatory and pathogenic roles of C5aR1 and C5aR2 in acute pyelonephritis with different specific mechanisms, that is, C5a/C5aR1 axis contributes to renal inflammation and tissue damage through mediating excessive inflammation and possibly providing potential binding site for Escherichia coli on renal tubular epithelial cells (RTECs), while C5a/C5aR2 axis through upregulation of HMGB1 and NLRP3 inflammasome in Mφs [18, 19]. This evidence concerns the gene C5AR2 and urinary tract infection.